miR-324-5p Contributes to Cell Proliferation and Apoptosis in Pancreatic Cancer by Targeting KLF3

Wan, Yicong; Luo, Haitao; Yang, Ming; Xia, Tian; Peng, Bo; Zhan, Ting; Chen, Xiaoli; Ding, Yu; He, Ju-Liang; Cheng, Xiaohuan; Huang, Xiaodong; Zhang, Yadong

doi:10.1016/j.omto.2020.07.011

Cited by 23 publications

(15 citation statements)

References 42 publications

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“…According to in vitro and in vivo research, KLF3 inhibition accelerates lung cancer EMT and promotes lung cancer metastasis through the STAT3 signalling pathway [ 26 ]. Overexpression of KLF3 suppressed cell proliferation and increased apoptosis in vitro, and it has also been demonstrated to be downregulated in human pancreatic cancer [ 27 ]. In our study, KLF3 expression levels in human CRC were shown to be lower than in normal tissues, and the results of univariate and multivariate Cox regression analysis suggested that KLF3 was associated with a better prognosis in CRC patients.…”

Section: Discussionmentioning

confidence: 99%

Expression and Prognosis Value of the KLF Family Members in Colorectal Cancer

Huang

Qiu

et al. 2022

Journal of Oncology

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Krüppel-like factors (KLFs) are some kind of transcriptional regulator that regulates a broad range of cellular functions and has been linked to the development of certain malignancies. KLF expression patterns and prognostic values in colorectal cancer (CRC) have, however, been investigated rarely. To investigate the differential expression, predictive value, and gene mutations of KLFs in CRC patients, we used various online analytic tools, including ONCOMINE, TCGA, cBioPortal, and the TIMER database. KLF2-6, KLF8-10, KLF12-15, and KLF17 mRNA expression levels were dramatically downregulated in CRC tissues, but KLF1, KLF7, and KLF16 mRNA expression levels were significantly elevated in CRC tissues. According to the findings of Cox regression analysis, upregulation of KLF3, KLF5, and KLF6 and downregulation of KLF15 were linked with a better prognosis in CRC. For functional enrichment, our findings revealed that KLF members are involved in a variety of cancer-related biological processes. In colon cancer and rectal cancer, KLFs were also shown to be associated with a variety of immune cells. The findings of this research reveal that KLF family members’ mRNA expression levels are possible prognostic indicators for patients with CRC.

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Section: Discussionmentioning

confidence: 99%

Expression and Prognosis Value of the KLF Family Members in Colorectal Cancer

Huang

Qiu

et al. 2022

Journal of Oncology

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“…MiR‐324‐5p has been reported to regulate cell proliferation and apoptosis under diverse conditions by targeting different mRNAs (Wang et al , 2015 ; Lin et al , 2018 ; Chen et al , 2019b ; Wan et al , 2020 ; Zheng et al , 2021 ). For example, miR‐324‐5p inhibits mitochondrial fusion and apoptosis in cardiomyocytes and endothelial progenitor cells by downregulating Mtfr1 (Wang et al , 2015 ; Chen et al , 2019b ; Huang et al , 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Interferon‐mediated repression of miR ‐324‐5p potentiates necroptosis to facilitate antiviral defense

Dou

et al. 2022

EMBO Reports

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Mixed lineage kinase domain‐like protein (MLKL) is the terminal effector of necroptosis, a form of regulated necrosis. Optimal activation of necroptosis, which eliminates infected cells, is critical for antiviral host defense. MicroRNAs (miRNAs) regulate the expression of genes involved in various biological and pathological processes. However, the roles of miRNAs in necroptosis‐associated host defense remain largely unknown. We screened a library of miRNAs and identified miR‐324‐5p as the most effective suppressor of necroptosis. MiR‐324‐5p downregulates human MLKL expression by specifically targeting the 3′UTR in a seed region‐independent manner. In response to interferons (IFNs), miR‐324‐5p is downregulated via the JAK/STAT signaling pathway, which removes the posttranscriptional suppression of MLKL mRNA and facilitates the activation of necroptosis. In influenza A virus (IAV)‐infected human primary macrophages, IFNs are induced, leading to the downregulation of miR‐324‐5p. MiR‐324‐5p overexpression attenuates IAV‐associated necroptosis and enhances viral replication, whereas deletion of miR‐324‐5p potentiates necroptosis and suppresses viral replication. Hence, miR‐324‐5p negatively regulates necroptosis by manipulating MLKL expression, and its downregulation by IFNs orchestrates optimal activation of necroptosis in host antiviral defense.

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“…For example, exogenous miR-93-5p promotes EC cell proliferation and communication by targeting Pten. MiR-324-5p may promote the progression of thyroid, oropharyngeal, pancreatic, and lung cancer cells, polarized M2 macrophages in colon cancer, and modulated the microenvironment in thyroid cancer ( Wan et al, 2020 ). However, the functions of miR-324-5p in EC remain unclear.…”

Section: Discussionmentioning

confidence: 99%

Construction of a Nine-MicroRNA-Based Signature to Predict the Overall Survival of Esophageal Cancer Patients

Zhang

et al. 2021

Front. Genet.

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BackgroundEsophageal cancer (EC) is a common malignant tumor. MicroRNAs (miRNAs) play a key role in the occurrence and metastasis and are closely related to the prognosis of EC. Therefore, it will provide a powerful tool to predict the overall survival (OS) of EC patients based on miRNAs expression in EC tissues and blood samples.MethodsFive independent databases, TCGA, GSE106817, GSE113486, GSE122497, and GSE112264, were used to construct nine-miRna signature and nomograms for prognosis. The bioinformatics analysis was used to predict the enrichment pathways of targets.ResultsA total of 132 overexpressed miRNAs and 23 suppressed miRNAs showed significant differential expression in both EC serum and tissue samples compared with normal samples. We also showed that nine miRNAs were related to the prognosis of EC. Higher levels of miR-15a-5p, miR-92a-3p, miR-92a-1-5p, miR-590-5p, miR-324-5p, miR-25-3p, miR-181b-5p, miR-421, and miR-93-5p were correlated to the shorter survival time in patients with EC. In addition, we constructed a risk prediction model based on the levels of nine differentially expressed miRNAs (DEMs) and found that the OS time of EC patients with high-risk score was shorter than that of EC patients with low-risk score. Furthermore, our results showed that the risk prediction scores of EC samples were higher than those of normal samples. Finally, the area under the curve (AUC) was used to analyze the risk characteristics of EC and normal controls. By calculating the AUC and the calibration curve, the RNA signature showed a good performance. Bioinformatics analysis showed that nine DEMs were associated with several crucial signaling, including p53, FoxO, PI3K-Akt, HIF-1, and TORC1 signaling. Finally, 14 messenger RNAs (mRNAs) were identified as hub targets of nine miRNAs, including BTRC, SIAH1, RNF138, CDC27, NEDD4L, MKRN1, RLIM, FBXO11, RNF34, MYLIP, FBXW7, RNF4, UBE3C, and RNF111. TCGA dataset validation showed that these hub targets were significantly differently expressed in EC tissues compared with normal samples.ConclusionWe have constructed maps and nomograms of nine-miRna risk signals associated with EC prognosis. Bioinformatics analysis revealed that nine DEMs were associated with several crucial signaling, including p53, FoxO, PI3K-Akt, HIF-1, and TORC1 signaling, in EC. We think that this study will provide clinicians with an effective decision-making tool.

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miR-324-5p Contributes to Cell Proliferation and Apoptosis in Pancreatic Cancer by Targeting KLF3

Cited by 23 publications

References 42 publications

Expression and Prognosis Value of the KLF Family Members in Colorectal Cancer

Expression and Prognosis Value of the KLF Family Members in Colorectal Cancer

Interferon‐mediated repression of miR ‐324‐5p potentiates necroptosis to facilitate antiviral defense

Construction of a Nine-MicroRNA-Based Signature to Predict the Overall Survival of Esophageal Cancer Patients

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